The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
DNMT3A and TET2 dominate clonal hematopoiesis and demonstrate benign phenotypes and different genetic predispositions
Open accessAbstract
had no impact on blood counts or indices. Mutational burden of both genes correlated with X-inactivation skewing but no significant association with age-adjusted telomere length reduction was documented. The discordance between the high prevalence of mutations in these 2 genes and their limited biological impact raise the question of the potential role of dysregulated epigenetic modifiers in normal aging hematopoiesis, which may include support to failing hematopoiesis.
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“Other studies have found links between CHIP and chronic obstructive pulmonary disease (COPD) 37,63.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [63]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Various other systemic effects have been described in association with CH, including chronic obstructive pulmonary disease and other pulmonary disease [16,33,34]”
From Clonal hematopoiesis and inflammation – the perpetual cycle (2023) · cites this paper as [33]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Loss-of-function heterozygous mutations in epigenetic regulators DNMT3A (cytosine methyltransferase) and TET2 (methylcytosine dioxygenase) are the most frequently detected mutations in CHIP, accounting for about 50% to 60% and 10% to 30% of mutations found in CHIP carriers, respectively.1, 2, 3,7,8”
From Aging drives Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In the context of CHIP, TET2 mutations show highest clonal expansion rates over time (with an estimated 10% annual growth rate compared with 5% of DNMT3A mutations7,8,10).”
From Aging drives Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Loss-of-function heterozygous mutations in epigenetic regulators DNMT3A (cytosine methyltransferase) and TET2 (methylcytosine dioxygenase) are the most frequently detected mutations in CHIP, accounting for about 50% to 60% and 10% to 30% of mutations found in CHIP carriers, respectively.1, 2, 3,7,8”
From Aging drives Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [7]
Experimental — accuracy not yet measured
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In the citing paper
“are predicted to have high expansion rates (10% increase in mean VAF per year1, 2, 3,7)”
From Aging drives Tet2 +/− clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [7]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“many have noted that DNMT3A mutations confer little phenotype on steady state hematopoiesis (Buscarlet et al., 2017)”
From Chronic infection drives Dnmt3a-loss-of-function clonal hematopoiesis via IFNγ signaling (2021) · cites this paper as Buscarlet et al., 2017
In the citing paper
“CHIP itself does not denote a malignancy, nor is it associated with clinically significant alterations in blood counts 28,63.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [63]
In the citing paper
“However, CHIP was also strongly linked to smoking in these studies, so the result could be confounded by this association.”
From Clonal hematopoiesis in human aging and disease (2019) · cites this paper as [63]
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Citations
Cites
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Telomere measurement by quantitative PCR
Cawthon, R. (2002) · Nucleic Acids Research · doi:10.1093/nar/30.10.e47 · Cited by 3,550
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Genovese, G., Kähler, A. K., Handsaker, R. E., Lindberg, J., Rose, S. A., Bakhoum, S. F., Chambert, K., Mick, E., Neale, B. M., Fromer, M., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1409405 · Cited by 3,531
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The origin and evolution of mutations in acute myeloid leukemia
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Identification of pre-leukaemic haematopoietic stem cells in acute leukaemia
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Cited by
Sorted by citations
Clonal hematopoiesis in human aging and disease
Jaiswal, S., & Ebert, B. L. (2019) · Science · doi:10.1126/science.aan4673 · Cited by 1,156
“Other studies have found links between CHIP and chronic obstructive pulmonary disease (38, 64).”
Prediction of acute myeloid leukaemia risk in healthy individuals
Abelson, S., Collord, G., Ng, S. W. K., Weissbrod, O., Mendelson Cohen, N., Niemeyer, E., Barda, N., Zuzarte, P. C., Heisler, L., Sundaravadanam, Y., et al. (2018) · Nature · doi:10.1038/s41586-018-0317-6 · Cited by 850
Molecular Minimal Residual Disease in Acute Myeloid Leukemia
Jongen‐Lavrencic, M., Grob, T., Hanekamp, D., Kavelaars, F. G., Hinai, A. S. A. A., Zeilemaker, A., Erpelinck-Verschueren, C. A. J., Gradowska, P. L., Meijer, R. J., Cloos, J. J., et al. (2018) · New England Journal of Medicine · doi:10.1056/nejmoa1716863 · Cited by 804
Sano, S., Oshima, K., Wang, Y., MacLauchlan, S., Katanasaka, Y., Sano, M., Zuriaga, M. A., Yoshiyama, M., Goukassian, D., Cooper, M. A., et al. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.12.037 · Cited by 699
Somatic mutations precede acute myeloid leukemia years before diagnosis
Desai, P., Mencia-Trinchant, N., Savenkov, O., Simon, M. S., Cheang, G., Lee, S., Samuel, M., Ritchie, E. K., Guzman, M. L., Ballman, K. V., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0081-z · Cited by 619
Metadata
- Authors
- Buscarlet, M., Provost, S., Zada, Y. F., Barhdadi, A., Bourgoin, V., Lépine, G., Mollica, L., Szuber, N., Dubé, M.-P., & Busque, L.
- Affiliations
- Hôpital Maisonneuve-Rosemont (CA)
- Montreal Heart Institute (CA)
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2017-08-10
- Volume
- 130
- Issue
- 6
- Pages
- 753-762
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2728241634
- Cited by
- 383
- References
- 50
- Citations by year
- 2026: 22 · 2025: 34 · 2024: 37 · 2023: 47 · 2022: 59 · 2021: 55 · 2020: 46 · 2019: 40 · 2018: 34 · 2017: 6
- FWCI
- 26.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Concordia University
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- DNMT3A, TET2, clonal hematopoiesis, somatic mutations, X-inactivation skewing, telomere length, epigenetic regulators, genetic susceptibility, mutational burden
- MeSH terms
- DNA Methyltransferase 3A, Age Factors, Aged, Aged, 80 and over, Aging, Blood Cell Count, Clone Cells, DNA (Cytosine-5-)-Methyltransferases, DNA-Binding Proteins, Female, Hematopoiesis, Humans, Male, Middle Aged, Mutation, Proto-Oncogene Proteins, Cohort Studies, Hematologic Neoplasms, Genetic Predisposition to Disease, Dioxygenases, X Chromosome Inactivation, High-Throughput Nucleotide Sequencing, Telomere Homeostasis
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